New research kills the MRSA ‘superbug’
A large number of fighters have been stricken with MRSA (methicillin resistant staphylococcus aureus) including King Mo, Ken Shamrock, Kevin Randleman, among many others. The result is often a hole in your body. Don’t google for images.
MRSA is not simply a plague for fighters, it is one of the leading public health threats of our time.
The potent bacterium’s resistance to antibiotics has kept it one step ahead of researchers. Until now.
A groundbreaking study published Wednesday in the journal Nature by Northeastern University Professor of Biology Kim Lewis, promises a novel method to treat and eliminate MRSA.
The so-??called “superbug” infects 1 million Americans each year. A major problem with MRSA is the development of deep-??seated chronic infections such as osteomyelitis (bone infection), endocarditis (heart infection), or infections of implanted medical devices. Once established, these infections are often incurable, even when appropriate antibiotics are used.
Bacteria such as MRSA have evolved to actively resist certain antibiotics, a fact that has generated significant interest among the scientific and medical communities. But Lewis, Director of Northeastern’s Antimicrobial Discovery Center, suspected that a different adaptive function of bacteria might be the true culprit in making these infections so devastating.
The new work represents the culmination of more than a decade of research on a specialized class of cells produced by all pathogens called persisters. According to Lewis, these cells evolved to survive. “Survival is their only function,” he said. “They don’t do anything else.”
Lewis and his research team posited that if they could kill these expert survivors, perhaps they could cure chronic infections—even those resistant to multiple antibiotics such as MRSA. Furthermore, said Brian Conlon, a postdoctoral researcher in Lewis’ lab and first author on the paper, “if you can eradicate the persisters, there’s less of a chance that resistance will develop at all.”
Lewis found that persisters achieve their singular goal by entering a dormant state that makes them impervious to traditional antibiotics. Since these drugs work by targeting active cellular functions, they are useless against dormant persisters, which aren’t active at all. For this reason, persisters are critical to the success of chronic infections and biofilms, because as soon as a treatment runs its course, their reawakening allows for the infection to establish itself anew.
In the recent study, Lewis’ team found that a drug called ADEP effectively wakes up the dormant cells and then initiates a self-??destruct mechanism. The approach completely eradicated MRSA cells in a variety of laboratory experiments and, importantly, in a mouse model of chronic MRSA infection.
Coupling ADEP with a traditional antibiotic, Conlon noted, allowed the team to completely destroy the bacterial population without leaving any survivors.
As with all other antibiotics, actively growing bacterial cells will likely develop resistance to ADEP. However, Lewis said, “cells that develop ADEP resistance become rather wimpy.” That is, other traditional drugs such as rifampicin or linezolid work well against ADEP-??resistant cells, providing a unique cocktail that not only kills persisters but also eliminates ADEP-??resistant mutant bacteria.
While ADEP targets MRSA, Lewis’ team believes similar compounds will be useful for treating other infections as well as any other disease model that can only be overcome by eliminating a population of rogue cells, including cancerous tumors. They are pursuing several already.